Evidence map›Paper›PMID 24064688›Full record

ArticleThe Journal of clinical endocrinology and metabolism2013

Increased AKT or MEK1/2 activity influences progesterone receptor levels and localization in endometriosis.

Jennifer L Eaton, Kenji Unno, Marshall Caraveo, Zhenxiao Lu, J Julie Kim

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 2 pooled it
7.3field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Review
  6. Dietary Caloric Restriction Suppresses Endometriosis by Inhibiting STAT3/ERK Pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. The long road of drug development for endometriosis - Pains, gains, and hopes.Journal of controlled release : official journal of the Controlled Release Society · 2024
    Review
  12. Review
  13. Association betweenCurrent issues in molecular biology · 2024
    Article
  14. Review
  15. Article
  16. Review
  17. Strategies for modelling endometrial diseases.Nature reviews. Endocrinology · 2022
    Review
  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Jennifer L EatonPhD, Department of Obstetrics and Gynecology, Robert H. Lurie Comprehensive Cancer Center, 303 East Superior, Room 4-117, Northwestern University, Chicago, Illinois 60611. j-kim4@northwestern.edu.
Kenji Unno
Marshall Caraveo
Zhenxiao Lu
J Julie Kim
Northwestern University · US

Funding

Regulation of IGFBP-1 by FKHR and HOXA10 in pregnancyR01HD044715 · NICHD · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KIM, JI-YONG JULIE · 2003 to 2010
$1.8M
NICHD NIH HHS R01 HD044715NICHD NIH HHS R01HD044715
6 · The paper itself

Abstract

contextEndometriosis is characterized by progesterone resistance and hyperactivity of the AKT and MAPK pathways. Kinases can cause posttranslational modifications of the progesterone receptor (PR) to influence cellular localization and protein stability.

objectiveThe objective of this study was to determine whether the increased AKT or MAPK kinase-1/2 (MEK1/2) activity observed in endometriotic stromal cells (OSIS) from ovarian endometriomas influences levels of PR protein. In turn, the effects of inhibiting AKT or MEK1/2 in the presence of the progestin R5020 on cell viability were investigated.

resultsInhibiting AKT with MK-2206 or MEK1/2 with U0126 for 24 hours in the absence of R5020 increased total and nuclear PRA and PRB protein levels in OSIS but not in eutopic endometrial stromal cells from disease-free patients from disease-free patients. MK-2206 and R5020 decreased OSIS viability and increased apoptosis. Trends toward decreased volumes of sc grafted endometriosis tissues were demonstrated with MK-2206 and progesterone.

conclusionsInhibition of AKT or MEK1/2 increased total and nuclear PR protein in OSIS. MK-2206 and R5020 decreased OSIS viability and increased apoptosis. The AKT and MAPK pathways may be potential molecular targets for the treatment of endometriosis.

Indexed as

Signal TransductionAdultApoptosisCell NucleusCells, CulturedCell SurvivalEndometriosisFemaleHumansMitogen-Activated Protein Kinase KinasesOvarian DiseasesOvaryProgestinsProtein IsoformsProtein Kinase InhibitorsProtein TransportMitogen-Activated Protein Kinase KinasesProgestinsProtein IsoformsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktReceptors, Progesterone

Identifiers

PMID24064688
PMCPMC3849681
OpenAlexW2083063093

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.